RRC ID 46501
Author Singhvi A, Teuliere J, Talavera K, Cordes S, Ou G, Vale RD, Prasad BC, Clark SG, Garriga G.
Title The Arf GAP CNT-2 regulates the apoptotic fate in C. elegans asymmetric neuroblast divisions.
Journal Curr Biol
Abstract During development, all cells make the decision to live or die. Although the molecular mechanisms that execute the apoptotic program are well defined, less is known about how cells decide whether to live or die. In C. elegans, this decision is linked to how cells divide asymmetrically [1, 2]. Several classes of molecules are known to regulate asymmetric cell divisions in metazoans, yet these molecules do not appear to control C. elegans divisions that produce apoptotic cells [3]. We identified CNT-2, an Arf GTPase-activating protein (GAP) of the AGAP family, as a novel regulator of this type of neuroblast division. Loss of CNT-2 alters daughter cell size and causes the apoptotic cell to adopt the fate of its sister cell, resulting in extra neurons. CNT-2's Arf GAP activity is essential for its function in these divisions. The N terminus of CNT-2, which contains a GTPase-like domain that defines the AGAP class of Arf GAPs, negatively regulates CNT-2's function. We provide evidence that CNT-2 regulates receptor-mediated endocytosis and consider the implications of its role in asymmetric cell divisions.
Volume 21(11)
Pages 948-54
Published 2011-6-7
DOI 10.1016/j.cub.2011.04.025
PII S0960-9822(11)00441-6
PMID 21596567
PMC PMC3109113
MeSH ADP-Ribosylation Factor 1 / physiology ADP-Ribosylation Factor 6 ADP-Ribosylation Factors / physiology Animals Apoptosis* Caenorhabditis elegans / cytology* Caenorhabditis elegans / genetics Caenorhabditis elegans / metabolism Caenorhabditis elegans Proteins / genetics Caenorhabditis elegans Proteins / metabolism Caenorhabditis elegans Proteins / physiology* Cell Division / physiology* Cell Polarity Endocytosis / genetics GTPase-Activating Proteins / genetics GTPase-Activating Proteins / metabolism GTPase-Activating Proteins / physiology*
IF 9.601
Times Cited 14
C.elegans tm2328 tm1447